Naringenin’s Function In Improving Learning And Memory Ability Of Model Rats With Alzheimer Disease Through The Approach Of Oxidative Stress

ObjectivesTo investigate the effects of naringenin on the learning and memoryability of Alzheimer disease (AD) rats.Methods40male SD rats were randomly divided into control group, modelgroup, naringenin low dose group(25mg/kg), naringenin middle dosegroup(50mg/kg) and naringenin high dose group(100mg/kg),8rats in eachgroup. Rats in model group and naringenin group were injectedstreptozotocin（3mg/kg）twice into each of two intracerebroventriculas tobuild AD model rats. Then, three naringenin groups were given intragastricadministration of naringenin once a day for3weeks and the other twogroups were, instead, given intragastric administration of normal saline withthe same dosage and time period. After3weeks，testing rats’ learning andmemory ability in all rats by Morris water maze and then extracting the rats’ brain tissue. Observing the expressions of Aβ-42and Aβ-40byimmunohistochemical method. Quantifying the expression and the degree ofphosphorylation of tau protein by western blotting. At last,measuring theactivity of superoxide dismutase (T-SOD) and the content ofmalondialdehyde (MDA) of the rats’ brain tissue by chemical colorimetricdetermination.Results1. Comparing with the control group, the mean escape latency of themodel group was significantly prolonged (p＜0.05) and the time that ratswere in the platform quadrant was significantly shortened (p＜0.05). On thecontrary, comparing with the model group, the mean escape latency of threenaringenin groups was significantly shortened (p＜0.05) and the time thatrats were in the platform quadrant was significantly extended (p＜0.05).2.The expressions of Aβ-42and Aβ-40in model group were obviously morethan those in the control group. Instead, the expressions of Aβ-42and Aβ-40in the naringenin middle dose group were significantly less than those in themodel group.3. There was no significant difference in the expression of tauprotein among each groups. Nevertheless, the phosphorylation of tau proteinin the model group was significantly increased than that in the control group(p＜0.05), and the phosphorylation of tau protein in the naringenin middlegroup was significantly reduced than that in the model group(p＜0.05).4.The content of MDA in the model group, comparing with the control group, was significantly enhanced(p＜0.05). Whereas, the content in naringeninmiddle group, comparing with the model group, was significantly decreased(p＜0.05). Besides, the activity of SOD in the model group was obviouslydecreased comparing with the control group (p＜0.05), yet the activity ofSOD in the naringenin middle group was obviously increased comparingwith the model group (p＜0.05).ConclusionNaringenin can improve learning and memory ability of model ratswith Alzheimer disease through the approach of oxidative stress.